- This document presents 3 case scenarios of neonatal jaundice. The first case involves a 2-day old female infant with a serum bilirubin of 272 referred for poor breastfeeding and phototherapy. The second case involves a 10-day old male infant referred for jaundice and weight loss with a bilirubin of 310. The third case involves a 25-day old male infant with a history of jaundice and admissions with a current bilirubin of 356.
Multidisciplinary case chronic myelogenous leukemia in pregnancyDR MUKESH SAH
Pregnancy and CML
While pregnancy in and of itself does not affect the course of CML, there is a risk for maternal disease progression if CML remains untreated for the duration of pregnancy. Unfortunately, treatment of CML during pregnancy is complicated due to the teratogenic nature of TKIs
Multidisciplinary case chronic myelogenous leukemia in pregnancyDR MUKESH SAH
Pregnancy and CML
While pregnancy in and of itself does not affect the course of CML, there is a risk for maternal disease progression if CML remains untreated for the duration of pregnancy. Unfortunately, treatment of CML during pregnancy is complicated due to the teratogenic nature of TKIs
Failure to thrive in neonates and infants + pediatric case.pptxclaviclebrown44
Hello, I’m Dr. Mariam Abayomi, an Intern doctor in Jamaica, passionate about promoting health and wellbeing. I invite you to explore my latest presentation on Failure to Thrive (FTT), a condition that can significantly impact a child’s growth and development.
In this presentation, you'll learn about:
- Understanding FTT: What is Failure to Thrive? We’ll break down the medical definition, common causes, and symptoms to watch for.
- Case Study Insight: Meet [Child’s Name], a [age]-month-old who struggled with FTT. Through their story, we’ll explore the real-life application of diagnosing and managing this condition.
- Diagnostic Approaches: From growth charts to lab tests, discover the essential tools and methods used to identify FTT.
- Management and Treatment: Learn about the multidisciplinary strategies employed to help children with FTT thrive, including nutritional support, medical treatments, and family education.
- Key Takeaways: Highlighting the importance of early detection, comprehensive care, and ongoing monitoring to ensure the best outcomes for children.
By following me on social media @HealthInspire, you’ll get updates, tips, and insights into health and wellbeing. Whether you’re a healthcare professional, a student, or a parent, my goal is to provide you with reliable information, support, and a bit of humor to navigate the world of health and wellness.
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Lecture on DKA in pregnancy - presented at JGH Obstetrics & Gynaecology Teaching Jan 2020. Fictional details have been used to anonymise any resemblance to persons living or passed.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
2. Case scenario 1
⚫Para 1 at 38w 5d. Blood group: A positive. Pregnancy uneventful
⚫DOB: 27/10/19 at 2338H. CTSH15. G6PD: normal. BW 2.71kg.
CW:2.43kg. Female
⚫Noted on day2 of life prior to discharge, baby jaundice. Was given
follow up at KK. Blood taken at 60 H of life at KK SBV:272 ( IPL: 274,
CPL: 224) with weight loss 10.3% due to poor breastfeeding technique,
thus referred to hospital.
⚫Baby was on intensive phototherapy for 6H
3. ⚫Investigation:
⚪ Hb16.2/ Hct 44.2 TWC 12.6/
Plt 456/ ANC 6
29/10 at KK 30/10 31/10
Urea 9 6
K 4.4 4.2
Na 143 139
Creat 60 43
T.Bili 272 178 125
D.Bili 10 5 6
Direct % 3.7% 2.8% 4.8%
(IPL/CPL) 274/224 291/241 325/275
4. ⚫ Further history:
⚪ Baby has minimal regurgitation 20-30 min post feeding, no vomiting.
⚪ Breast feeding technique poor with duration 60 minutes per session.mother claim sucking
present and good.
⚫ Imp: neonatal jaundice secondary to inadequate feeding
⚫ Upon discharge, breast milk inadequate, but able to EBM and breast feeding
technique acceptable.
⚫ Pt was discharged well on 31/10/19 with Syr. Domperidone 1mg QID and T.
domperidone 10mg TDS (for mother) and TCA to review weight
5. Case scenario 2.
A 10 days old baby boy was referred from KK for neonatal jaundice and weight
loss 11.7%. His t.bil 310. Photo level IPL 359 , CPL309
Further history?
⚫ Para 1 at 39w 1d.Mother’s blood group: B positive. Pregnancy uneventful. SVD
⚫ G6PD normal. CTSH 4. BW:3.68kg. CW 3.25kg. HC 34cm. Lt 52cm.
⚫ 2nd hospitalisation: admitted on D4 of life for NNJ requiring single phototherapy
and discharged on next day.
⚫ Tolerating BFOD every 2 hours, 45minutes each session. Mother claim baby content
after each session. Good sucking. Claim breast milk adequate
⚫ BO yellowish stool (2-3 times/day). PU regularly,yellowish urine ( 8-9 times/day)
⚫ Fever?
6. Examination?
⚫O/E: active, AF soft, not tachypneic, jaundice till abdomen, good pulse
volume, warm peripheries, pink
⚫P/A: soft, not distended. Liver and spleen not palpable.
⚫SBV at KK: 241- 265- 287- 310
⚫Differential Diagnosis?
8. ⚫Futher history:
⚪ Mother do EBM post feeding ( 2oz) and threw away
⚫Imp:
1. severe jaundice
2. prolonged jaudice
3.Weight loss secondary inadequate calorie intake
9. Case scenario 3
⚫Para 1 at 38w 3d.Mother’s blood group: AB positive. SVD
⚫ANC:
⚫ Teenage pregnancy
⚫ late booker
⚫Baby boy .G6PD normal. CTSH 4. BW:2.88kg. CW 3.25kg. HC 34cm.
Lt 52cm.
⚫3rd hospitalisation:
⚫ 1) H/o NNJ at D5 of life, admitted 3 days. Highest SBV requiring intensive
phototherapy for a day.
⚫ 2) H/o admission at D12 oflife for 3 days for idiopathic jaundice. weight upon
discharge: 2.6kg
10. ⚫ Baby was referred from KK on D25
of life. Noted SBV 356 ( IPL: 358/
CPL: 308)
⚫ Tolerating BFOD every 2 hours,
30minutes each session. Mother
claim baby content after each
session.
⚫ BO yellowish stool (7-8
times/day). PU regularly,yellowish
urine , not reducing in amount.
⚫ Baby active as usual. Mother
claimed no traditional
medication/Food given.
⚫ CW: 3.125kg ( weight gain 50g/d
since discharge)
⚫ O/E: no significant
findingsFurther history:
⚪ Father and paternal siblings have
G6PD deficiency
⚪ Both parents negative for thalassemia
screening
⚪ No h/0 neonatal death in family
⚪ imp: rebound prolonged jaundice for
investigation
11. 24/7 25/7 27/7 29/7 31/7
HB 13.2 12.6 10.7 10.2
HCT 36.5 35.1 29.1 28.3
TWC 7.1 7.6 8.3 7.0
PLT 369 358 375 382
ANC 3 1 1.3 1.08
Urea 2.4 1.3
K 5.4 5.3
Na 140 139
Creat 42 42
TP 50
Alb 31
T.Bili 302 290 252 211 157
D.Bili 50 39 29 20 19
Direct % 16% 13% 11.5% 9.5% 12%
⚫ CRP 0.3/ ammonia 47
⚫ Lactate 2.6- 3.5- 3.7- 1.9
⚫ LDH 335 -310-301-296
⚫ Reticulocyte 1.2%
⚫ Urine reducing sugar: negative
⚫ PBF: occasional spherocytes seen
TRO recent hemolysis
⚫ Infective screening : non reactive
⚫ UFEME: negative
⚫ Urine C+S: mixed growth with 2
types of gram positive cocci abd 1
type gram negative rod
⚫ Blood group : AB positive. Coombs
test negative
12. ⚫Imp:
⚪ Unconjugated hyperbilirubinemia
⯍ Parents not keen for Gilbert syndrome screening d/t financial issue
⚪ Treat as UTI
⚫Subsequently, pt was discharged well and given TCA to review IEM
result
14. INTRODUCTION
⚫ Jaundice is the yellow discoloration of
skin, sclerae, and other tissues caused
by the deposition of bilirubin.
⚫ Jaundice is clinically detectable when
serum bilirubin more than 85ʮmol/L
(5mg/dL)
15. Why does newborn more prone to jaundice?
High hemoglobin mass at birth
Shorter fetal hemoglobin life
span
Low enzyme Glucuronyltransferase activity
(reach adult level by 14 days regardless of gestation)
Low concentration of ligandin Y protein
(carries unconjugated bilirubin to the smooth
endoplasmic reticulum) – increase to adult level by
5-10 days of age
Excessive bilirubin
production
Poor bilirubin
clearance
Liver immaturity
.
19. Risk factors of severe NNJ
⚫ prematurity
⚫ low birth weight
⚫ jaundice in the first 24 hours of life
⚫ mother with Blood Group O or Rhesus Negative
⚫ G6PD deficiency
⚫ rapid rise of total serum bilirubin
⚫ sepsis
⚫ lactation failure in exclusive breastfeeding
⚫ high predischarge bilirubin level
⚫ cephalhaematoma or bruises
⚫ babies of diabetic mothers
⚫ family history of severe NNJ in siblings
.
21. Time frame for jaundice
DAY 1 DAY 7 DAY14(TERM)/DAY21(PRETERM)
22. CAUSES OF JAUNDICE
< 24 HOURS OF AGE 24 HOURS - 2 WEEKS OF AGE > 2 WEEKS OF AGE
HAEMOLYTIC DISORDERS • Physiological jaundice
• Breast milk jaundice
• Infection: e.g. UTI
• Haemolytic disorders
• Bruising
• Polycythemia
• Crigler-Najjar syndrome
UNCONJUGATED
• Rhesus incompatibility
• ABO incompatibility
• G6PD deficiency
• Spherocytosis
• Pyruvate kinase deficiency
• Septicaemia
• Breast milk jaundice
• Hypothyroidism
• Haemolytic
anaemia,G6PD/spherocytosi
s
• Pyloric stenosis
• Galactosemia and Gilbert
CONGENITAL INFECTIONS CONJUGATED
• Toxoplasmosis
• CMV
• HSV
• Rubella
• Bile duct obstruction
• Biliary atresia
• Choledochal cyst
• Sclerosing cholangitis
• Neonatal hepatitis
• TORCHES
23. 1. Age of onset
2. Age of gestation
3. Associated symptoms of jaundice
4. Birth history
5. Feeding history
6. Drug and allergy history
7. Family history
HISTORY TAKING ON NEONATAL JAUNDICE
24. ⚫Preterm (<37 weeks)
⚫Term (>37 weeks)
⚫ The incidence of hyperbilirubinaemia increases with
decreasing gestational age.
⚫ Preterm infants are more susceptible to damage from
raised bilirubin.
AGE OF GESTATION
25. ASSOCIATED SYMPTOMS OF JAUNDICE
•General symptoms
• Yellow skin
• Yellow eye
• Sleepiness
• Decrease in activity
• Difficulty in feeding
• Vomiting
•Intestinal obstruction
•Infection
• Fever
• Rashes
Biliary tract obstruction
• Brown dark urine
• Pale stool
Kernicterus
• Irritabilty
• Fits
• Coma
• Abnormal posture
Hypothyroidism
• Reduced activity
History of falls / trauma
26. BIRTH HISTORY
• ANTENATAL HISTORY
• Mother’s blood group
• Rhesus
isoimmunization
• Intrauterine infection :
TORCHES
• GDM, PIH
• Polycythemia
• INTRAPARTUM
HISTORY
• Birth trauma
• Method of delivery
Instrumental delivery
(forceps /
Ventousse)
• POSTPARTUM HISTORY
• Birth weight
• Loss of weight in the
following days
• APGAR / spontaneous cry
• Asphyxia / HIE / Liver
infarction
• NICU admission
• Neonatal jaundice
• Phototherapy given
• G6PD status
• Cord TSH result
27. • Breast milk jaundice
• (first 4-7 days of life in a
breastfed newborn)
• Contents of breast milk inhibiting
conjugating enzyme in liver
• Breast feeding jaundice
• (first 3 days of life in a
breastfed newborn)
• Insufficient intake of breast milk -
dehydration
FEEDING HISTORY
28. • Drug taken by mother during breastfeeding?
• Any traditional medication taken?
• Any medication taken by baby?
• Any known allergy?
DRUG AND ALLERGY HISTORY
29. • Hemolytic disease
• Previous infants with
• neonatal jaundice
• kernicterus
• G6PD deficiency
FAMILY HISTORY
30. PHYSICAL EXAMINATION
⚫ General condition:
⚫ weight, hydration status, sign of sepsis
⚫ signs of acute bilirubin encephalopathy
(ABE), should be assessed fo all babies with
severe NNJ
⚫ Severity of jaundice
⚫ Sign of kernicterus:
⚫ lethargy, hypotonia, seizure,
opisthotonus,retrocollis, high pitch cry
⚫ Pallor, plethora, SAH, cephalhaematoma
⚫ Sign of intra-uterine infection: petechiea,
hepatospelnomegaly
31.
32. Cephalocaudal progression
FACE > NECK > CHEST > ABDOMEN
> LIMBS
⚫ Visual assessment, Kramer’s rule
⚫ Transcutaneous bilirubinometer- if
Tcb level > 200umol/l, TSB should
be obtained. Not to be used for
patient on phototherapy
⚫ Total serum bilirubin
Method of detecting jaundice
33. INVESTIGATIONS
1. SBV on admission
2. SBV monitoring: if CPL, SBV cm; if IPL / near ET level, SBV 6 hourly
3. If mother’s blood group is O+ve / Rhesus –ve: ABO Coombs
In babies with severe hyperbilirubinaemia, early-onset
neonatal jaundice (<24 hours) or rapid rise of TSB (>8.5
µmol/L/h)
1. FBC, Retic count +/- peripheral blood picture
2. RP if significant weight loss
3. If prolonged jaundice: full LFT, TFT, UFEME, Urine C&S
4. Septic workup: Blood C&S, CRP (if infection is suspected)
5. G6PD screening (if not done)
35. Indications for referral to hospital
• Jaundice within 24 hours of life
• Jaundice below umbilicus (200-250 µmol/L)
• Jaundice extending to soles of feet (urgent referral – sign of severe NNJ)
• Family history of significant haemolytic disease or kernicterus
• Any unwell infant with jaundice
• Prolonged jaundice of >14 days
• Conjugated hyperbilirubinemia
36. Treatment
Phototherapy
• Mainstay of treatment in NNJ.
• Phototherapy should be commenced when
total serum bilirubin reaches the
phototherapy threshold for neonatal
jaundice.
• Conventional phototherapy: minimum
irradiance of 15uW/cm2/nm.
• Intensive phototherapy: minimum
irradiance of 30uw/cm2/nm
37. •position the light source - 35-50cm from top surface of the infant
expose infant adequately-cover eyes
monitor serum bilirubin levels as indicated
monitor infant’s temperature 4 hourly to avoid chilling or overheating
ensure adequate hydration and good urine output. adjust fluid(oral)
accordingly.
Routine fluid supplementation is not required with good temperature homeostasis
discontinue phototherapy when serum bilirubin is below phototherapy level
38.
39.
40. Exchange Transfusion
⚫ Indication
⚪ lower serum bilirubin level and reduce the risk of brain damage associated with
kernicterus
⚫ Volume to be exchanged is 2x the infant’s total blood volume (2x80mls/kg)
⚫ Use Fresh Whole Blood preferably < 5 days old
⚫ Connect baby to a cardiac monitor
⚫ Cannulate the umbilical vein
⚫ Aliquot for removal and replacement – 5-6 mls/ kg (Not more than 5-8% of blood volume)
⚫ Maximum volume per cycle - 20 mls for term infants, ≤ 5 ml/kg for ill or preterm infants
⚫ Rate of exchange: 3 -4 minutes per cycle (1 minute ‘out’, 1 minute ‘in’, 1-2 minute ‘pause’
excluding time to discard blood and draw from blood bag)
41.
42. Measures to prevent severe neonatal jaundice
• promote successful breastfeeding (at least 8-10 times/24hours)
• observe infants with G6PD deficiency, for at least 5days if not jaundice and
longer if moderate jaundice
• mother with blood group O and with a sibling who had severe neonatal
jaundice - observe the infant for at least the first 24 hours of life
• infants with hemolytic disease, if phototherapy is initiated early and
discontinued before the infants is 3-4 days old , monitor for rebound
jaundice and adequacy of breast feeding within the next 24-48hours
43. Follow up
• All infants discharged <48hours after birth should be seen within 2-3 days of
discharge
• Infants with risk factors for severe neontal jaundice , early follow up to detect
rebound jaundice after discharge
• Infants with serum bilirubin >20mg/dl and those require exchange transfusion
should be followed for neurodevelopment outcome
• Do a hearing assessment(using BAEP) at 0-3months of corrected age
• Brainstem auditory evoked potential (BAEP)
44. References
1. Malaysian Paediatric Protocol 4th edition.
2. Management of Neonatal Jaundice (2nd edition), Clinical Practice Guideline
Malaysia.
3. Ullah, S., Rahman, K., & Hedayati, M. (2016). Hyperbilirubinemia in Neonates:
Types, Causes, Clinical Examinations, Preventive Measures and Treatments: A
Narrative Review Article. Iranian journal of public health, 45(5), 558–568.
4. Kramer LI. Advancement of Dermal Icterus in the Jaundiced Newborn. Amer J
Dis Child. 1969; 118: 454-458.